The control of gene expression will be studied in two separate host-virus systems. (1) Following infection of E. coli by bacteriophage T7, host transcription is suppressed by the action of a phage-coded protein kinase which phosphorylates the bacterial RNA polymerase. Preliminary evidence indicates that the inactivation of the polymerase is the results of its association with an inhibitor. We intend to characterize the properties of the inhibitor, and the role of the protein kinase in promoting its association with the polymerase. (2) Synthesis of RNA from the late genes of bacteriophage T7 is mediated by a phage-specified RNA polymerase; two temporal classes of RNA have been observed. In part, regulation of transcription is the result of virus induced changes in membrane permeability. We plan to characterize this novel regulatory mechanism. (3) Subviral (core) particles of vaccinia virus contain an endogenous RNA polymerase which may be activated in vitro. By hybridizing transcription products to restriction fragments of vaccinia DNA, we intend to compare the in vitro products to those made in vivo during virus infection.